Fragile X mental retardation is the most common form of inherited mental disorders, and occurs due to the loss of a single gene, FMR. In Drosophila, it was revealed that dFMR plays a role in modulating circadian locomotor behavior. dFMR is phosphorylated by CK2, and loss of this kinase also impairs function of the clock. While aspects of the core transcriptional feedback loop that drives the clock have been well defined, little is known about the way in which the clock communicates timing information. We hypothesize that dfmr and CK2 interact in vivo and that dfmr function in Drosophila pacemaker neurons influences output of the circadian clock. To test these ideas in vivo behavioral, genetic, and molecular investigations of the interaction between dFMR and CK2 will be employed. Results of this study may uncover an example of dfmr regulation in the circadian rhythm pathway and provide novel means of adjusting circadian outputs to modulate sleep and other daily rhythms. Moreover, analysis of dfmr will bring about increased understanding of the function, and consequence of loss, of this disease gene, potentially leading to unique interventions in Fragile X mental retardation.